Abstract

Abstract

Lepromatous tissue from armadillos inoculated 24–36 months earlier with Mycobacterium leprae was obtained for electron microscopic studies. Cytochemically stained lepromas revealed a subpopulation of macrophages containing peroxisomes. These peroxidase reactive macrophages were not infected with bacilli. Acid phosphatase was present in macrophages and many of these were infected with bacilli and contained vacuoles and lipid globules. Within the membrane-bound vacuoles, acid phosphatase surrounded bacilli. However, the reaction product ended abruptly at a 15–40 millimicron thick zone of low electron density surrounding intact bacilli. Acid phosphatase was more intensely reactive and localized less precisely in heavily infected and vacuolated macrophages than in lightly and non-infected cells. The effectiveness of this bacillary barrier and the numerous infected macrophages with substantial acid phosphatase argue against the ability of acid phosphatase to protect host cells from leprosy bacilli. Evidence suggests a protective action of peroxidase or the rapid turnover of macrophages within lepromas. Granular and membranous debris were commonly seen within vacuoles of infected macrophages. A portion of the debris was ultrastructurally similar to bacillary matrix and was nonreactive for peroxidase and acid phosphatase. Following homogenization and centrifugation, similar materials banded with bacilli above 60% sucrose. Another portion of the debris was ultrastructurally similar to host lysosomal matrix and was reactive for acid phosphatase. Results support the concept of dual host and parasitic origins of the debris found in phagolysosomes of infected macrophages. Transparent, oval Epon defects remained eccentric to the majority of intact bacilli in centrifuged fractions. Apparently, an intrinsic property of leprosy produced these Epon defects.